Purpose: We studied the sleep macroarchitecture with polysomnography (PSG) in drug naïve patients with Parkinson′s disease (PD) and reassessed them following treatment with levodopa. Materials and ...Methods: This prospective hospital-based study included 15 patients with PD (age: 59 ± 11.2 years, duration of PD: 11.8 ± 12.3 months; and male: female (M:F) = 11:4). They were assessed for demography, phenotype, modified Hoehn and Yahr staging (H & Y); Schwab and England and Activities of Daily Living (S and E ADL) Scale; and Unified PDRating Scale (UPDRS). Sleep was assessed using Epworth Sleepiness Scale (ESS), Pittsburgh Sleep Quality Index (PSQI), and National Institute of Mental Health and Neurosciences (NIMHANS) comprehensive sleep disorder questionnaire. They underwent overnight PSG at baseline and after13.3 ± 5.7 months of levodopa (440 mg/day). Results: Patients with PD had responded to levodopa as indicated by the significant improvement in UPDRS motor score in ON state compared to OFF state. Nocturnal sleep quality indices did not vary significantly, but the excessive daytime somnolence improved (P = 0.04) with levodopa. Sleep efficiency (P = 0.65), latency to sleep onset (P = 0.19), latency to stage 1 (P = 0.12), and duration of stage 1 (P = 0.55) had increased. Duration of ′awake in bed′ (P = 0.24), slow wave sleep (P = 0.29), and rapid eye movement (REM) sleep (P = 0.24) decreased with treatment. Periodic leg movements (PLMs) had reduced (P = 0.68) and mean oxygen saturation during sleep improved (P = 0.002). Surprisingly, snore index (P < 0.03) during sleep had increased with levodopa. Conclusions: Sleep alterations in PD occur even in early stages due to the disease process. There was improvement in most of the parameters of sleep macroarchitecture with levodopa.
Full text
Available for:
IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
Background: Amyotrophic lateral sclerosis (ALS) is a relatively rare neurological disorder affecting upper and lower motor neurons in the brain and spinal cord with survival for 3-5 years and rarely ...beyond 10 years. Sleep disturbances in ALS are underreported and undertreated and there is no related data from India. This study aimed to assess the frequency of sleep disorders in patients of ALS and their determinants.
Methods: Patients with definite and probable ALS as per the El Escorial criteria were recruited from May 2014 to April 2016. Functional impairment, presence of sleep specific abnormalities and anxiety and depression were assessed using standardized questionnaires.
Results: Forty patients with ALS (23 male; 17 female) with their median age at presentation being 58.5 years (range 44-75 years) and the median duration of illness being 18 months (range: 4-120 months) were includedin the study. Half of the patients had poor sleep quality, which was significantly worse across all components of Pittsburgh Sleep Quality Index (PSQI) compared to controls. Sleep disorders were observed in 70%, insomnia in 65%, sleep disordered breathing/hypoventilation in 52.5% and restless legs syndrome in 5% patients. Night time awakenings attributable to symptoms associated with ALS were noted in 85%, and anxiety and depression in 57.5% patients. Excessive daytime somnolence emerged as an independent predictor for the presence of sleep disorders in ALS patients on multivariate logistic regression P = 0.043, odd's ratio (OR) 1.435; 95% confidence intervalCI (1.011-2.036).
Conclusion: This is the first study from India providing insight into the presence of sleep disorders in ALS. About half of the patients of ALS had a poor sleep quality and two-thirds suffered from sleep disturbances.
Full text
Available for:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, UILJ, UKNU, UL, UM, UPUK
Objective: We studied the changes in Polysomnographic (PSG) profile in drug-naïve patients of Parkinson′s disease (PD) who underwent evaluation with sleep overnight PSG. Materials and Methods: This ...prospective study included 30 with newly diagnosed levodopa-naïve patients with PD, fulfilling the UK-PD society brain bank clinical diagnostic criteria (M:F = 25:5; age: 57.2 ± 10.7 years). The disease severity scales and sleep related questionnaires were administered, and then patients were subjected to overnight PSG. Results: The mean duration of illness was 9.7 ± 9.5 months. The mean Hoehn and Yahr stage was 1.8 ± 0.4. The mean Unified Parkinson′s Disease Rating Scale (UPDRS) motor score improved from 27.7 ± 9.2 to 17.5 ± 8.9 with sustained usage of levodopa. Nocturnal sleep as assessed by Pittsburgh Sleep Quality Index (PSQI) was impaired in 10 (33.3%) patients (mean PSQI score: 5.1 ± 3.1). Excessive day time somnolence was recorded in three patients with Epworth Sleepiness Scale (ESS) score ≥ 10 (mean ESS score: 4.0 ± 3.4). PSG analysis revealed that poor sleep efficiency of <85% was present in 86.7% of patients (mean: 68.3 ± 21.3%). The latencies to sleep onset (mean: 49.8 ± 67.0 minutes) and stage 2 sleep (36.5 ± 13.1%) were prolonged while slow wave sleep was shortened. Respiration during sleep was significantly impaired in which 43.3% had impaired apnoea hyperpnoea index (AHI) ≥5, mean AHI: 8.3 ± 12.1). Apnoeic episodes were predominantly obstructive (obstructive sleep apnea, OSA index = 2.2 ± 5.1). These patients had periodic leg movement (PLM) disorder (56.7% had PLM index of 5 or more, mean PLMI: 27.53 ± 4 9.05) that resulted in excessive daytime somnolence. Conclusions: To conclude, sleep macro-architecture is altered in frequently and variably in levodopa-naοve patients of PD and the alterations are possibly due to disease process per se.
Full text
Available for:
IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
Cerebral venous thrombosis (CVT) is an uncommon but potentially fatal condition which presents with a wide range of symptoms. Some of these presenting features are vague thus contributing to the ...delay in diagnosis. A prompt diagnosis and initiation of appropriate therapy are therefore of paramount importance. In this pictorial, we have tried to illustrate the direct and indirect imaging features of CVT in detail on multiple imaging modalities, along with the potential pitfalls of imaging.
Full text
Available for:
EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
A 63-year-old man with type 2 diabetes mellitus, alcohol consumption in moderation, and three episodes of hepatic encephalopathy presented with symmetrical lower limb distal weakness, sensory ataxia, ...thickened palpable nerves, mood disturbances for seven years, and a family history of schizophreniform disorders. Nerve conduction studies showed demyelinating sensorimotor polyradiculoneuropathy. CSF analysis showed mild albumino-cytological dissociation. MRI brain and lumbosacral plexus showed thickened fifth cranial nerves and lumbosacral roots. He was treated with steroids for a provisional diagnosis of chronic inflammatory polyneuropathy and became encephalopathic. EEG showed triphasic waves. Serum ammonia was 201 micrograms/dL. Further evaluation suggested ornithine transcarbamylase (OTC) deficiency. The patient underwent hemodialysis with a low protein diet, rifaximin, and sodium benzoate, with subsequent recovery.
•Awareness of hyperammonemia and urea cycle defects is must prior to initiation of immunotherapy.•Recurrent encephalopathy and familial psychiatric disorders suggest late onset urea cycle defects.•Sensory ataxic polyneuropathy maybe a rare manifestation of late OTC deficiency.
Full text
Available for:
GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Antiphospholipid syndrome (APS), an autoantibody mediated disease, is characterized by presence of antibodies against the proteins bound to the phospholipid membranes. The antibodies are ...predominantly formed against beta-2-glycoprotein I (b2GPI) which is considered pathogenic, but presence of lupus anticoagulant is a predictor of thrombotic events. The thrombotic events in APS may manifest as venous or arterial or small vessel thrombosis in any tissue or organ and pregnancy related complications namely, recurrent (three or more) and early spontaneous miscarriages before 10 weeks of gestation or unexplained deaths of normal fetus at or beyond 10 weeks, eclampsia or severe pre-eclampsia, intra-uterine growth retardation and pre-term births. However, lately its role as an etiological mechanism in causation of certain neuro-psychiatric disorders has been put forth. It has been suggested that one should suspect APS in psychiatric manifestations which are atypical, resistant to treatment, associated with cognitive decline and dementia, abnormal involuntary movements, livedo reticularis, migraine, thrombotic events like stroke or transient ischemic attacks, obstetrical complications. In this brief communication, we describe the case of young male who has been suffering from treatment resistant and difficult to manage bipolar affective disorder (BPAD) with fluctuating thrombocytopenia and neurological findings with positive lupus anticoagulant. We propose it to be a consequence of an atypical presentation of APS.
•Antiphospholipid syndrome (APS) is being researched as a possible etiopathogenetic mechanism in certain neuro-psychiatric disorders.•APS must be suspected in cases with atypical presentations, resistance to treatment, presence of cognitive decline and dementia.•Presence of abnormal involuntary movements, livedo reticularis, headaches, stroke, transient ischemic attacks must raise suspicion of APS.•Observe caution in managing young patients with atypical psychiatric symptoms, treatment resistance, neurological or hematological symptoms.•Caution should be observed while managing young patients with atypical psychiatric presentations who are treatment resistant and have neurological and hematological symptoms.
Full text
Available for:
GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
PDF
